Angiotensin II Type 1a Receptor Is Involved in the Occurrence of Reperfusion Arrhythmias

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Abstract
Background —A growing body of evidence has suggested that the renin-angiotensin system plays an important role in the development of cardiac hypertrophy induced by hemodynamic overload and left ventricular remodeling after myocardial infarction. The role of the renin-angiotensin system in ischemia-reperfusion (IR) injury, however, has not been established. Methods and Results —To determine the role of angiotensin II (Ang II) in IR injury, we examined infarct size and arrhythmias after IR using Ang II type 1a receptor (AT1a) knockout mice. The left coronary artery was occluded for 30 minutes followed by reperfusion for 120 minutes. There were no significant differences in infarct size between wild-type and knockout mice determined by dual staining with triphenyltetrazolium chloride and Evans blue dye. The number of ventricular premature beats after reperfusion in knockout mice, however, was much less than in wild-type mice. Treatment with a selective AT1 antagonist, CV-11974, before ischemia blocked reperfusion arrhythmias in wild-type mice but had no effects on infarct size. Conclusions —Ang II may be critically involved in the induction of ventricular arrhythmias but not in the determination of infarct size after IR.